title: Nicotinic acid treatment shifts the fibrinolytic balance favourably and decreases plasma fibrinogen in hypertriglyceridaemic men.
abstract: BACKGROUND
  Nicotinic acid in gram doses decreases cholesterol and triglyceride concentrations in plasma, but the effect on haemostatic function is not known.
  
  
  METHODS
  Twenty-three men with hypertriglyceridaemia were treated with 4 g nicotinic acid daily for 6 weeks. Tests for haemostatic function and serum lipoproteins were performed before and at the end of the period of treatment.
  
  
  RESULTS
  Treatment with nicotinic acid had the expected effect on lipoprotein concentrations: it reduced the serum concentrations of triglyceride and the three major density fractions of triglyceride (very low density lipoprotein (VLDL), low density lipoprotein (LDL) and high density lipoprotein (HDL)). The VLDL cholesterol concentration was reduced, but that of HDL cholesterol was increased (all P<0.0001). The lipoprotein(a) (Lp(a)) concentration decreased significantly (P<0.01). The total fibrinolytic activity was increased by nicotinic acid treatment as indicated by decreases in plasminogen activator inhibitor-1 activity from 34.3 to 23.8 U/ml (P<0.01) and in alpha2-antiplasmin activity from 1.10 to 0.97 U/ml (P<0.01). The plasma fibrinogen concentration decreased from 3.55 to 3.01 U/ml (P<0.01). Multvariate analysis showed that the changes in alpha2-antiplasmin and Lp(a) concentrations could explain 53% of the change in plasma fibrinogen, suggesting that increased plasmin mobilization could be responsible for the decrease in plasma fibrinogen.
  
  
  CONCLUSIONS
  This study of hypertriglyceridaemic men has shown that long-term treatment with nicotinic acid not only corrects serum lipoprotein abnormalities, but also reduces the fibrinogen concentration in plasma and stimulates fibrinolysis.
authors.affiliation: Research Centre of General Medicine, NVSO, Karolinska Hospital, Stockholm, Sweden.
authors.forename: J O
authors.initials: JO
authors.lastname: Johansson
authors.forename: N
authors.initials: N
authors.lastname: Egberg
authors.forename: A
authors.initials: A
authors.lastname: Asplund-Carlson
authors.forename: L A
authors.initials: LA
authors.lastname: Carlson
mesh_terms: D000284:Administration, Oral; D000328:Adult; D000368:Aged; D000704:Analysis of Variance; D001786:Blood Glucose / Q000187:drug effects; D004334:Drug Administration Schedule; D004797:Enzyme-Linked Immunosorbent Assay; D005340:Fibrinogen / Q000032:analysis*; D006487:Hemostasis / Q000187:drug effects; D006801:Humans; D015228:Hypertriglyceridemia / Q000097:blood* / Q000175:diagnosis / Q000188:drug therapy*; D008074:Lipoproteins / Q000032:analysis / Q000187:drug effects*; D008075:Lipoproteins, HDL / Q000032:analysis / Q000187:drug effects; D008079:Lipoproteins, VLDL / Q000032:analysis / Q000187:drug effects; D008297:Male; D008875:Middle Aged; D009525:Niacin / Q000008:administration & dosage*; D017395:Plasminogen Activator Inhibitor 1 / Q000032:analysis; D012044:Regression Analysis; D010959:Tissue Plasminogen Activator / Q000032:analysis / Q000187:drug effects; D016896:Treatment Outcome; D014841:von Willebrand Factor / Q000032:analysis / Q000187:drug effects
chemical_list: D001786:Blood Glucose; D008074:Lipoproteins; D008075:Lipoproteins, HDL; D008079:Lipoproteins, VLDL; D017395:Plasminogen Activator Inhibitor 1; D014841:von Willebrand Factor; D009525:Niacin; D005340:Fibrinogen; D010959:Tissue Plasminogen Activator